Chemotherapy-induced thrombocytopenia is caused by the decrease of megakaryocytes due to apoptosis of bone marrow stem cells and megakaryocytes (Kaushansky, K., The thrombocytopenia of cancer. Prospects for effective cytokine therapy. Hematol Oncol Clin North Am, 1996. 10(2): p. 431-55; Prow, D. and S. Vadhan-Raj, Thrombopoietin: biology and potential clinical applications. Oncology (Williston Park), 1998. 12(11): p. 1597-604, 1607-8; discussion 1611-4; Thiele, J., et al., Effects of the tyrosine kinase inhibitor imatinib mesylate(STI571) on bone marrow features in patients with chronic myelogenous leukemia. Histol Histopathol, 2004. 19(4): p. 1277-88; Lonial, S., et al., Risk factors and kinetics of thrombocytopenia associated with bortezomib for relapsed, refractory multiple myeloma. Blood, 2005. 106(12): p. 3777-84. To reduce thrombocytopenia, treatments aiming to increase stem cell proliferation and megakaryocytes differentiation have been examined. For the differentiation of megakaryocytes from stem cells, interleukins and thrombopoietin (TPO) play important roles (Kaluzhny, Y. and K. Ravid, Role of apoptotic processes in platelet biogenesis. Acta Haematol, 2004. 111(1-2): p. 67-77). Early clinical studies of interleukins (ILs) showed that they stimulated the formation of platelets directly or indirectly in patients with chemotherapy-induced thrombocytopenia (Vadhan-Raj, S., et al., Effects of interleukin-1 alpha on carboplatin-induced thrombocytopenia in patients with recurrent ovarian cancer. J Clin Oncol, 1994. 12(4): p. 707-14; Leonardi, V., et al., Interleukin 3 in the treatment of chemotherapy induced thrombocytopenia. Oncol Rep, 1998. 5(6): p. 1459-64; D'Hondt, V., et al., Thrombopoietic effects and toxicity of interleukin-6 in patients with ovarian cancer before and after chemotherapy: a multicentric placebo-controlled, randomized phase Ib study. Blood, 1995. 85(9): p. 2347-53; Gordon, M. S., et al., A phase I trial of recombinant human interleukin-11 (neumega rhIL-11 growth factor) in women with breast cancer receiving chemotherapy. Blood, 1996. 87(9): p. 3615-24; Tepler, I., et al., A randomized placebo-controlled trial of recombinant human interleukin-11 in cancer patients with severe thrombocytopenia due to chemotherapy. Blood, 1996. 87(9): p. 3607-14; Smith, J. W., 2nd, et al., The effects of treatment with interleukin-1 alpha on platelet recovery after high-dose carboplatin. N Engl J Med, 1993. 328(11): p. 756-61). However, the pleiotropic effect of ILs often results in side effects, including hyperbilirubinemia, anemia, fever, hypotension, headaches, and chills (Vadhan-Raj, S., et al., Effects of interleukin-1 alpha on carboplatin-induced thrombocytopenia in patients with recurrent ovarian cancer. J Clin Oncol, 1994. 12(4): p. 707-14; Smith, J. W., 2nd, et al., The effects of treatment with interleukin-1 alpha on platelet recovery after high-dose carboplatin. N Engl J Med, 1993. 328(11): p. 756-61; Gordon, M. S., et al., A phase I trial of recombinant human interleukin-6 in patients with myelodysplastic syndromes and thrombocytopenia. Blood, 1995. 85(11): p. 3066-76; Lazarus, H. M., et al., Phase I multicenter trial of interleukin 6 therapy after autologous bone marrow transplantation in advanced breast cancer. Bone Marrow Transplant, 1995. 15(6): p. 935-42; Nieken, J., et al., Recombinant human interleukin-6 induces a rapid and reversible anemia in cancer patients. Blood, 1995. 86(3): p. 900-5). Apoptosis inhibition in megakaryocytes has been examined previously (Srivastava, R. K., et al., Involvement of microtubules in the regulation of Bc12 phosphorylation and apoptosis through cyclic AMP-dependent protein kinase. Mol Cell Biol, 1998. 18(6): p. 3509-17; Yin, D. X. and R. T. Schimke, BCL-2 expression delays drug-induced apoptosis but does not increase clonogenic survival after drug treatment in HeLa cells. Cancer Res, 1995. 55(21): p. 4922-8; Biswas, R. S., et al., Inhibition of drug-induced Fas ligand transcription and apoptosis by Bcl-XL. Mol Cell Biochem, 2001. 225(1-): p. 7-20). Anti-apoptotic proteins such as Bcl-2, Bcl-XL, and caspase inhibitors were shown to be useful for protecting megakaryocytes from apoptosis (Kaluzhny, Y., et al., BclxL overexpression in megakaryocytes leads to impaired platelet fragmentation. Blood, 2002. 100(5): p. 1670-8; Ogilvy, S., et al., Constitutive Bcl-2 expression throughout the hematopoietic compartment affects multiple lineages and enhances progenitor cell survival. Proc Natl Acad Sci USA, 1999. 96(26): p. 14943-8); however, these commonly used anti-apoptosis treatments are not effective to prevent thrombocytopenia. It has been reported that (1) Bcl-2 and Bcl-xL reduced the production of platelets probably due to the inhibition of microtubule polymerization by Bcl-2 and Bcl-XL (Kaluzhny, Y., et al., BclxL overexpression in megakayocytes leads to impaired platelet fragmentation. Blood, 2002. 100(5): p. 1670-8; Ogilvy, S., et al., Constitutive Bcl-2 expression throughout the hematopoietic compartment affects multiple lineages and enhances progenitor cell survival. Proc Natl Acad Sci USA, 1999. 96(26): p. 14943-8), and (2) caspase inhibitors markedly decreased platelet formation because caspase activity is required for the release of platelets from megakaryocytes (De Botton, S., et al., Platelet formation is the consequence of caspase activation within megakaryocytes. Blood, 2002. 100(4): p. 1310-7). Thus, there is a need for new strategies to protect megakaryocytes from chemotherapy-induced apoptosis without interfering platelet formation activity of megakaryocytes.